Other Determinants of Susceptibility

Not so long ago, it was almost guaranteed that you would die of an infectious disease. In fact, had you been born just 150 years ago, your chances of dying of an infectious disease before you've reached the tender age of 5 would have been extremely high.
Since then, science has come a long way in understanding infectious diseases - what they are, how they spread, and how they can be prevented. But diseases like HIV/AIDS, Malaria, Tuberculosis, or the flu are still major killers worldwide, and novel emerging diseases are a constant threat to public health. In addition, the bugs are evolving. Antibiotics, our most potent weapon against bacterial infections, are losing their power because the bacteria are becoming resistant. In this course, we'll explore the major themes of infectious diseases dynamics.
After we’ve covered the basics, we'll be looking at the dynamics of the flu, and why we're worried about flu pandemics. We'll be looking at the dynamics of childhood diseases such as measles and whooping cough, which were once considered almost eradicated, but are now making a comeback. We'll explore Malaria, and use it as a case study of the evolution of drug resistance. We'll even be looking at social networks - how diseases can spread from you to your friends to your friends' friends, and so on. And of course we’ll be talking about vaccination too. We’ll also be talking about how mobile phones, social media and crowdsourcing are revolutionizing disease surveillance, giving rise to a new field of digital epidemiology. And yes, we will be talking about Zombies - not human zombies, but zombie ants whose brains are hijacked by an infectious fungus.
We're looking forward to having you join us for an exciting course!

SN

great course and its intensive learning . One might think its just another course . However, one needs to follow all the lectures and notes closely to be able to pass all their assignments .

AJ

Jan 25, 2016

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I thoroughly enjoyed this course and learned a great deal of information in the process. I found the interviews to be very helpful in bringing it all together for me. Thank you professors!

从本节课中

Hosts

The second module of the course covers host factors that determine the outcome of infection. We will first focus on host immunity and present both the general immune capabilities—the innate immune response—that are encoded in our genes and that provide the initial response to infection and the adaptive immune response, which arises from highly specialized cells that protect against a specific pathogen. You will then learn about the ways that pathogens circumvent these two types of immunity and consider other factors that can contribute to an individual becoming infected or diseased—including genetic factors, other microbes, and how social and emotional factors influence immunity. We will then consider how infection with a microorganism causes disease and how public health officials determine whether a disease outbreak is caused by an infectious organism.

Dr. Rachel A. Smith

Dr. Mary L. Poss

Dr. David P. Hughes

Dr. Peter Hudson

Dr. Matthew Ferrari

Assistant Professor of Biology

Dr. Andrew Read

Alumni Professor in the Biological Sciences, and Professor of Entomology

Dr. Marcel Salathé

Assistant Professor of Biology

脚本

The immune system plays a crucial role in determining whether or not you are susceptible to infection by an organism that can cause disease. But susceptibility is not only a matter of your immune system; other factors can play a role as well, either by directly influencing susceptibility, or by affecting how well the immune system can do its job. In this video I'd like to show you three important factors. The first factor I'd like to talk about is genetics. Probably, the textbook example is a gene that codes for a part of a protein called hemoglobin. Hemoglobin is found in red blood cells, where it carries oxygen from the lung to tissues and organs. A single nucleotide change in the DNA sequence of that gene changes the protein that the gene produce in a very interesting way. If you have mutation on both copies of the gene, remember that you have two copies of each gene, one from your mother and one from your father. If you have the mutation on both copies, you will have a disease called sickle cell anemia. This is not an infectious disease. But it can be painful, nevertheless. However, if you have the mutation and only one copy, then you do not have sickle cell anemia. But you're highly resistant to malaria. Although not 100%. Another intriguing example is resistance to norovirus. Norovirus infections cause viral gastroenteritis. Which is often, and mistakenly called stomach flu. It's highly contagious, and very unpleasant. With abdominal pain, vomiting, and diarrhea's typical symptoms. There's a gene called FUT2. And again, it's a single nucleotide change on that chain that affects your resistance to the most common strains of norovirus. In this particular case, you need mutation on both copies of the gene to be resistant. Now, I happen to know that I actually carry this mutation on both copies of that gene. I know this because I got myself genotyped. Let me show you. This is a screenshot from the service that I used to get genotyped. As you can see, I have the A nucleotide. A stands for adenin, at the relevant location on both copies, and that's why it says AA genotype. Two people I'm sharing genotypes with, including my colleague and fellow course instructor, Andew Reed, have the A nucleotide on one copy, and the G nucleotide on the other copy. Where G stands for guanine. Three other people with whom I'm sharing this information have the G nucleotide type on both copies. I've removed some names to protect identities. But as you can see, none of those people are genetically resistant to norovirus infection. In fact, my particular genotype makes me resistant to other types of infection too, not just to noroviruses. But some research indicates that because I have this genotype, I may be at higher risk for infection with several bacteria, as well as the influenza virus, so there's no free lunch here. In any case, I hope these two examples demonstrate that sometimes small genetic differences, can translate into big differences with respect to your risk of infection. The second factor is the microbiome. The microbiome is the entirety of all the microbes that live on and in you. Now, here's a remarkable fact. The microbial cells in your body out number your human cells by a factor of ten. So for each human cell, there are about ten microbial cells in you. Further, the micro biome is estimated to contain at least 100 times more genes than you, your own genome. So, from a genetic perspective, your body is more microbial than it is human. On the other hand, though, your microbiome is estimated to weigh less than a kilogram. In any case, scientists only recently begun to reveal what remarkable affect the microbiome has on human health. Some people suggest that we need to call it an organ. We are only beginning to understand how the microbiome effects our ability to deal with infectious diseases. But from the little that we do know, all signs are indicating that the effects are very large, potentially even larger than the effects of the genome For example, in a recent animal study, it was found that both the intensity of infection and the specific success of different parasite strains were mostly driven by the microbiome in the host, rather than by host genotype. Finally, the environment can play a big role, too. Nutrition is a well known factor to affect infectious disease outcomes. For example, vitamin a has long been understood to play a crucial role in immune regulation. A deficiency in vitamin A impairs both the innate and adaptive immune response to infection. What's worse, many common infections, in turn, lead to decreasing levels of vitamin A. Leading to a potentially vicious cycle. I want to finish with two important points. The first is that these three factors are not the only factors. There are many other factors at work, too, but these three are known to be very important. The other point is that none of these factors act in isolation, they all influence each other in complex ways, and we are still only understanding a fraction of it.